MiR-122 partly mediates the ochratoxin A-induced GC-2 cell apoptosis

• OTA treatment resulted in a dose-dependent increase apoptosis in GC-2 cells.
• OTA can impair the synthesis and processing of miRNAs in the cytoplasm.
• OTA induced GC-2 cell apoptosis by causing an increase of caspase-3 activity.
• MiR-122 may partly mediate the OTA-induced GC-2 cell apoptosis.
• New avenues to understand the mechanism of OTA-induced cytotoxicity

Ochratoxin A (OTA) is a mycotoxin which has been shown to be nephrotoxic, hepatotoxic, and immunotoxic to animals, and mainly exists in the mildew grain. MicroRNAs (miRNAs) regulate a wide variety of cellular processes. However, the toxic effects of OTA on the germ cell and whether miRNAs mediate the effects of OTA-induced GC-2 cell apoptosis are still not clear. In the present study, OTA treatment resulted in a dose-dependent increase apoptosis in GC-2 cells. MiR-122 was increased in the OTA-treated GC-2 cells. It showed that Bcl-w was down-regulated after OTA treatment, and caspase-3 was obviously activated. Cyclin G1 (CCNG1) was significantly decreased, and inversely the expression of p53 was increased. Inhibition of miR-122 partly relieved the OTA-induced GC-2 cell apoptosis. These results indicate that OTA induces GC-2 cell apoptosis by causing the increase of caspase-3 activity and that miR-122 partly mediates the OTA-induced cell apoptosis.